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miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells
MicroRNAs (miRNAs) post-transcriptionally regulate gene expression by targeting the 3′ untranslated region (UTR) of target genes, and serve diverse roles in cell proliferation, differentiation and apoptosis. However, the association between miR-16-2-3p and 3-phosphoinositide-dependent protein kinase...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365086/ https://www.ncbi.nlm.nih.gov/pubmed/30664182 http://dx.doi.org/10.3892/ijmm.2019.4070 |
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author | Han, Tao Wu, Ni Wang, Youjing Shen, Weimin Zou, Jijun |
author_facet | Han, Tao Wu, Ni Wang, Youjing Shen, Weimin Zou, Jijun |
author_sort | Han, Tao |
collection | PubMed |
description | MicroRNAs (miRNAs) post-transcriptionally regulate gene expression by targeting the 3′ untranslated region (UTR) of target genes, and serve diverse roles in cell proliferation, differentiation and apoptosis. However, the association between miR-16-2-3p and 3-phosphoinositide-dependent protein kinase-1 (PDPK1) in nonsyndromic cleft lip (NSCL) remains unclear. In the present study, a luciferase activity assay indicated that miR-16-2-3p negatively regulated PDPK1 in maxillary primordium mesenchymal cells (MPMCs). In addition, it was confirmed that the expression levels of miR-16-2-3p was markedly increased in cleft lip tissues compared with those in adjacent normal lip tissues. A negative correlation between miR-16-2-3p and PDPK1 in cleft lip tissues was observed. Furthermore, miR-16-2-3p inhibited cell proliferation and migration, and induced apoptosis of MPMCs via repressing PDPK1. Finally, miR-16-2-3p exerted its suppressive role in MPMCs by inhibiting the PDPK1/protein kinase B signaling pathway. These results indicate that miR-16-2-3p may inhibit cell proliferation and migration, and promote apoptosis in MPMCs through repression of PDPK1 and may be a potential target for future clinical prevention and treatment of NSCL. |
format | Online Article Text |
id | pubmed-6365086 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-63650862019-02-19 miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells Han, Tao Wu, Ni Wang, Youjing Shen, Weimin Zou, Jijun Int J Mol Med Articles MicroRNAs (miRNAs) post-transcriptionally regulate gene expression by targeting the 3′ untranslated region (UTR) of target genes, and serve diverse roles in cell proliferation, differentiation and apoptosis. However, the association between miR-16-2-3p and 3-phosphoinositide-dependent protein kinase-1 (PDPK1) in nonsyndromic cleft lip (NSCL) remains unclear. In the present study, a luciferase activity assay indicated that miR-16-2-3p negatively regulated PDPK1 in maxillary primordium mesenchymal cells (MPMCs). In addition, it was confirmed that the expression levels of miR-16-2-3p was markedly increased in cleft lip tissues compared with those in adjacent normal lip tissues. A negative correlation between miR-16-2-3p and PDPK1 in cleft lip tissues was observed. Furthermore, miR-16-2-3p inhibited cell proliferation and migration, and induced apoptosis of MPMCs via repressing PDPK1. Finally, miR-16-2-3p exerted its suppressive role in MPMCs by inhibiting the PDPK1/protein kinase B signaling pathway. These results indicate that miR-16-2-3p may inhibit cell proliferation and migration, and promote apoptosis in MPMCs through repression of PDPK1 and may be a potential target for future clinical prevention and treatment of NSCL. D.A. Spandidos 2019-03 2019-01-21 /pmc/articles/PMC6365086/ /pubmed/30664182 http://dx.doi.org/10.3892/ijmm.2019.4070 Text en Copyright: © Han et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Han, Tao Wu, Ni Wang, Youjing Shen, Weimin Zou, Jijun miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells |
title | miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells |
title_full | miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells |
title_fullStr | miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells |
title_full_unstemmed | miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells |
title_short | miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells |
title_sort | mir-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting pdpk1 in maxillary primordium mesenchymal cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365086/ https://www.ncbi.nlm.nih.gov/pubmed/30664182 http://dx.doi.org/10.3892/ijmm.2019.4070 |
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